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This study validated how STAT3 influences endometrial cancer (EC) phenotypes and mapped its regulatory mechanisms upstream and downstream. STAT3 expression in EC tissues was assessed by immunohistochemistry, and dual luciferase assays confirmed regulation between STAT3 and miR-26a/b-5p. Functional effects on HEC-1A cells were measured using CCK-8, scratch, and Transwell assays, while co-immunoprecipitation verified STAT3–CHI3L1/YKL-40 binding. Results showed high STAT3 associated with progression, miR-26a/b-5p directly targeting STAT3, STAT3 promoting proliferation, migration, and invasion, and STAT3 inducing YKL-40 expression.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/oncology-reports-56-effect-of-the-mir-26ab-5p-stat3-ykl-40-regulatory-axis-on-proliferation-migration-and-invasion-of-endometrial-cancer-cells/349199/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/oncology-reports-56-effect-of-the-mir-26ab-5p-stat3-ykl-40-regulatory-axis-on-proliferation-migration-and-invasion-of-endometrial-cancer-cells/349199.png","ImageObject",300,407,{"name":92,"@type":93},"Cart","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-27","2026-09-22",true,{"@type":102,"interactionType":103,"userInteractionCount":14},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What is the study’s primary goal regarding STAT3 in endometrial cancer?","Question",{"text":112,"@type":113},"To validate STAT3’s impact on endometrial cancer phenotype and to investigate upstream and downstream regulatory mechanisms, including its relationship with miR-26a/b-5p.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How did the researchers confirm the regulatory relationship between STAT3 and miR-26a/b-5p?",{"text":117,"@type":113},"Immunohistochemistry assessed STAT3 expression in EC tissues, and dual luciferase assays confirmed regulation between STAT3 and miR-26a/b-5p.",{"name":119,"@type":110,"acceptedAnswer":120},"What effects did STAT3 and miR-26a/b-5p have on EC cell behavior?",{"text":121,"@type":113},"Upregulated STAT3 enhanced HEC-1A cell proliferation, migration, and invasion, counteracting the inhibitory effects of miR-26a/b-5p on migration and invasion.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},349199,1790471510,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":14,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},18829141979164,"https://eur-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","ONCOLOGY REPORTS 56: 127, 2026  \nEffect of the miR‑26a/b‑5p‑STAT3‑YKL‑40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells  \n* * *  \nXINZHAO SUN , SHANSHAN LIN , XUEYAN ZHONG , YANLU LUO, JIAHUANG YANG and JIANGTAO FAN  \nDepartment of Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China  \nReceived September 30, 2025; Accepted April 6, 2026  \nDOI: 10. 3892/or.2026.9132  \nAbstract. The incidence of endometrial cancer (EC) is on the rise annually, emphasizing the importance of timely diagnosis and treatment. Signal transducer and activator of transcription 3 (STAT3) has been identified as a proto‑oncogene involved in multiple signaling pathways affecting various biological processes, especially in tumours. The aim of the present study was to validate the impact of STAT3 on EC phenotype and investigate its upstream and downstream regulatory mecha‑ nisms. Immunohistochemical analysis was conducted to assess STAT3 expression in EC tissues, followed by dual luciferase assays to confirm the regulatory relationship between STAT3 and microRNA (miR)‑26a/b‑5p. The effects of STAT3 and miR‑26a/b‑5p on HEC‑1A cell proliferation and metastasis were evaluated through Cell Counting Kit‑8 assays, cell scratch assays, and Transwell assays. Co‑immunoprecipitation assays verified the binding between STAT3 and chitinase‑3‑like protein 1 (CHI3L1, also known as YKL‑40) . The results demonstrated high STAT3 expression in EC, associated with disease progression. miR‑26a/b‑5p directly targeted STAT3 . Upregulated STAT3 enhanced HEC‑1A cell proliferation, migration, and invasion, counteracting the inhibitory effects of miR‑26a/b‑5p on cell migration and invasion. In addition, it was confirmed that STAT3 binds to and promotes the expres‑ sion of YKL‑40 . These findings contribute to clarifying the pathogenesis of EC.  \nCorrespondence to: Dr Jiangtao Fan, Department of Gynecology, The First Affiliated Hospital of Guangxi Medical University, 6 Shuangyong Road, Nanning, Guangxi 530021, P.R. China  \nE‑mail: [jt_fan2018@163.com](jt_fan2018@163.com)  \n*Contributed equally  \nAbbreviations: CHI3L1 and YKL‑40, chitinase‑3‑like protein 1; EC, endometrial cancer; JAK, Janus kinase; STAT3, signal transducer and activator of transcription 3; TILs, tumor‑infiltrating lymphocytes; VEGF, vascular endothelial growth factor  \nKey words: endometrial cancer, STAT3, microRNA‑26a‑5p, microRNA‑26b‑5p, chitinase‑3‑like protein 1  \nIntroduction  \nEndometrial cancer (EC) is a gynecological cancer character‑ ized by a rapidly increasing global incidence and associated mortality rate. According to statistics, there were over 420,000 new cases of corpus uteri cancer worldwide in 2022 (1) . While EC predominantly affects postmenopausal women, there is arising incidence among younger women. Early detection and diagnosis of EC at the low‑grade stage have been revealed tobe associated with a favorable prognosis, whereas diagnosis at the advanced stages has been associated with a reduced chance of survival (2,3) .  \nThe STAT3 protein with 770 amino acids regulates cell survival, differentiation, and proliferation. Notably, STAT3 has been shown to contribute to the development of cancers, such as myeloma, as well as breast and lung cancers due to its inherent ability to enhance proliferation and metastasis of tumor cells, as well as induce chemo‑resistance and immune suppression. In human cancers, over‑activation of STAT3 has been demon‑ strated tobe associated with dismal outcomes (4‑6). Specifically, STAT3 has been shown to regulate invasion, proliferation, drug resistance, and angiogenesis of EC cells. Research has estab‑ lished that angiogenesis is a crucial process in the development of tumors. Vascular cancer‑associated fibroblasts, which are components of the tumor microenvironment, facilitate angio‑ genesis by promoting the expression of vascular endothelialcadherin and Vimentin, as well as ","cbCaikiArR3gdRi6","https://ap.wps.com/l/cbCaikiArR3gdRi6","pdf",14825319,15,"English","# Abstract\n# Introduction\n## STAT3 in cancer progression\n## miRNAs and the STAT3 regulatory axis","[{\"question\":\"What is the study’s primary goal regarding STAT3 in endometrial cancer?\",\"answer\":\"To validate STAT3’s impact on endometrial cancer phenotype and to investigate upstream and downstream regulatory mechanisms, including its relationship with miR-26a/b-5p.\"},{\"question\":\"How did the researchers confirm the regulatory relationship between STAT3 and miR-26a/b-5p?\",\"answer\":\"Immunohistochemistry assessed STAT3 expression in EC tissues, and dual luciferase assays confirmed regulation between STAT3 and miR-26a/b-5p.\"},{\"question\":\"What effects did STAT3 and miR-26a/b-5p have on EC cell behavior?\",\"answer\":\"Upregulated STAT3 enhanced HEC-1A cell proliferation, migration, and invasion, counteracting the inhibitory effects of miR-26a/b-5p on migration and invasion.\"}]","ONCOLOGY REPORTS - 56 - Effect of the miR-26a/b-5p-STAT3-YKL-40 regulatory axis on proliferation, migration, and invasion of endometrial cancer cells | PDF",1790082172,38]